GSK3β Controls mTOR and Prosurvival Signaling in Neurons

Autor: Iwona A. Cymerman, Fred Van Leuven, Malgorzata Urbanska, Agata Gozdz, Matylda Macias, Herman Devijver, Ilona Kondratiuk, Ewa Liszewska, Jacek Jaworski, Benoit Lechat
Rok vydání: 2017
Předmět:
0301 basic medicine
Regulator
Apoptosis
mTORC1
mTORC2
Neuronal survival
Glycogen synthase kinases-3
TEMPORAL-LOBE EPILEPSY
Phosphorylation
IN-VIVO
Cells
Cultured

Neurons
Ribosomal Protein S6
Mammalian target of rapamycin
Kainic Acid
TOR Serine-Threonine Kinases
CONDITIONAL TRANSGENIC MICE
CORTICAL-NEURONS
INDUCED SEIZURES
Brain
Cell Differentiation
PROTEIN TRANSLATION
Cell biology
Isoenzymes
Crosstalk (biology)
Neurology
Signal transduction
Life Sciences & Biomedicine
Signal Transduction
Cell Survival
LYSOSOMAL ACIDIFICATION
Neuroscience (miscellaneous)
Mice
Transgenic

Biology
Neuroprotection
CELL-PROLIFERATION
03 medical and health sciences
Cellular and Molecular Neuroscience
Animals
Excitotoxicity
PI3K/AKT/mTOR pathway
Science & Technology
Glycogen Synthase Kinase 3 beta
HIPPOCAMPAL-NEURONS
RPTOR
Neurosciences
030104 developmental biology
MAMMALIAN TARGET
nervous system
Neurosciences & Neurology
Proto-Oncogene Proteins c-akt
Zdroj: Molecular Neurobiology. 55:6050-6062
ISSN: 1559-1182
0893-7648
Popis: Glycogen synthase kinases-3β (GSK3β) is a key regulator of cell homeostasis. In neurons, GSK3β contributes to control of neuronal transmission and plasticity. Despite extensive studies in non-neuronal cells, crosstalk between GSK3β and other signaling pathways remains not well defined in neurons. In the present study, we report that GSK3β positively affected the activity of effectors of mammalian target of rapamycin complex 1 (mTORC1) and complex 2 (mTORC2), in mature neurons in vitro and in vivo. GSK3β also promoted prosurvival signaling and attenuated kainic acid-induced apoptosis. Our study identified GSK3β as a positive regulator of prosurvival signaling, including the mTOR pathway, and indicates the possible neuroprotective role of GSK3β in models of pharmacologically induced excitotoxicity. ispartof: MOLECULAR NEUROBIOLOGY vol:55 issue:7 pages:6050-6062 ispartof: location:United States status: published
Databáze: OpenAIRE